The 1990 research criteria for Fibromyalgia syndrome (FM) characterized this disorder by the presence of widespread pain combined and tenderness at 11 or more of 18 specific ‘tender points’. These criteria have been used for clinical diagnosis until the development of recent criteria that include the Widespread Pain Index (WPI) and the Symptom Severity (SS) scale that evaluates symptoms such as fatigue, sleep impairment and different autonomic symptoms (Wolfe et al., 1990, 2011). There is no consensus regarding the various mechanisms underlying the set of symptoms reported by FM sufferers.
An emerging body of evidence provides support for an important interaction between pain processing and cardiorespiratory regulatory systems (Bruehl & Chung, 2004; Maixner, 1991; Randich & Maixner, 1984; Maixner et al., 1995). It is generally accepted that the stimulation of carotid sinus and cardiopulmonary baroreceptor afferents, which are activated by dynamic changes in cardiovascular and respiratory parameters, reduce the magnitude of perceived pain. This attenuation of pain is mediated by activation of endogenous pain inhibitory systems, including central nervous system processes that inhibit activity in the ascending reticular activating system (ARAS), a non-specific cortical projecting system. The ARAS plays an important role in sculpting sensory, motor, and autonomic responses to somatosensory input (Steriade 1988, Steriade and Llinas 1988). In healthy individuals, a functional interaction of the cardiovascular and pain regulatory systems has been established whereby elevation in resting arterial blood pressure is related to reduction in pain sensitivity. The activation of carotid sinus and cardiopulmonary afferents attenuates perceived pain.
Recent studies have also shown that persistent pain conditions may be mediated in part by impairments in this interaction between blood pressure and pain sensitivity (Thieme & Turk, 2006). Diminished baroreceptor sensitivity may have an important impact on pain chronicity (Maixner 1997; Bruehl & Chung, 2004); Bruehl et al., 1998).
It is desired to provide non-pharmacological methods and devices for reducing chronic and acute pain.